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1 es, which was blocked by the ECE-1 inhibitor phosphoramidon.
2  metal chelator, and the elastase inhibitor, phosphoramidon.
3 tely reversed by treatment of the cells with phosphoramidon.
4 l/L phosphoramidon but not by 0.1 micromol/L phosphoramidon.
5 nzymatic activity was partially inhibited by phosphoramidon.
6 t and augmented by the ectoenzyme inhibitor, phosphoramidon.
7 roL) improved learning, which was blocked by phosphoramidon (1 and 10mM, respectively).
8                                 Intravitreal phosphoramidon (10(-3) M, n = 6) injection also resulted
9 hibiting either endogenous ET-1 release with phosphoramidon (10(-5) mol/L) or its action with PD14506
10 uble Abeta42, an effect which was blocked by phosphoramidon (10mM).
11                    In CHF patients (n = 10), phosphoramidon (a combined ECE and neutral endopeptidase
12  Cytotoxicity of CPI-0004Na was inhibited by phosphoramidon, a known inhibitor of CD10 enzymatic acti
13                                              Phosphoramidon, a neprilysin inhibitor, attenuated these
14 l, but not by amastatin plus captopril or by phosphoramidon alone, indicating that released opioids a
15                                 In contrast, phosphoramidon, an inhibitor of endothelin-converting en
16 .19 with the neutral endopeptidase inhibitor phosphoramidon and to -7.3 +/- 0.20 with captopril and p
17  an inhibitor of ET-converting enzyme (ECE), phosphoramidon, and were exposed to a 100% oxygen breath
18 ses sensitive to inhibition by thiorphan and phosphoramidon are especially important, because these i
19 helin-converting enzyme-1 (ECE-1) inhibitor, phosphoramidon, as well as a novel ET-1 receptor A antag
20 cted by an inhibitor of endopeptidase-24.11, phosphoramidon at 10(-6) M, which suggests that the tran
21 inhibited markedly by 0.1 and 100 micromol/L phosphoramidon at pH 5.4 (IC50 1.5 nmol/L), consistent w
22 30 micromol/L PD159790 and by 100 micromol/L phosphoramidon but not by 0.1 micromol/L phosphoramidon.
23 ved dynorphin A-induced internalization, and phosphoramidon, but not captopril, increased this effect
24 ell lines with the metalloprotease inhibitor phosphoramidon causes a 2-3-fold elevation in extracellu
25 idon and to -7.3 +/- 0.20 with captopril and phosphoramidon combined.
26                                We found that phosphoramidon decreased the apparent Bmax from 7.3 to 5
27                                 In contrast, phosphoramidon did not significantly affect the reductio
28 dase (captopril), and neutral endopeptidase (phosphoramidon) dramatically increased the potencies of
29 R-positive tumors, peptidase inhibition with phosphoramidon greatly enhanced B1R visualization in viv
30  enzyme was acted upon by the NEP inhibitors phosphoramidon (IC(50), 0.64 microM) and thiorphan (IC(5
31 ium supplemented with the protease inhibitor phosphoramidon indicated that the (125)I-ANP was mostly
32 inhibiting endothelin-converting enzyme with phosphoramidon normalized retinal blood flow in diabetic
33 ffect of the neutral endopeptidase inhibitor phosphoramidon on the binding of bradykinin to dog skele
34 ptidase inhibitors (amastatin, captopril and phosphoramidon) onto the lumbar spinal cord.
35  inhibition of endothelin-converting enzyme (phosphoramidon or SM19712).
36 ther inhibition of ET-1-converting enzyme by phosphoramidon (PA) would attenuate rejection in a rat m
37 ction of the neutral endopeptidase inhibitor phosphoramidon (PA), we were able to provoke remarkable
38 , an endothelin-converting enzyme inhibitor, phosphoramidon (PA, 10 mg/kg/day), or low-dose CsA + PA.
39   The effect of veratridine was protected by phosphoramidon plus amastatin or captopril, but not by a
40 Treatment of these double-knockout mice with phosphoramidon resulted in elevations of Abeta, suggesti
41 olog neprilysin 2 (NEP2), which is thiorphan/phosphoramidon-sensitive and degrades Abeta.
42 d) in Abeta, indicating that other thiorphan/phosphoramidon-sensitive endopeptidases are at work.
43 42 oligomers and enhances learning through a phosphoramidon-sensitive metalloproteinase-dependent mec
44  mRNA levels of endogenous fly NEP genes and phosphoramidon-sensitive NEP activity declined during ag
45 tors of metalloendopeptidases (thiorphan and phosphoramidon), serine proteinases (aprotinin), cystein
46 ptor antagonism (BQ123), and ECE inhibition (phosphoramidon, SM19712) or by inhibiting exocytosis (TA
47                                Thiorphan and phosphoramidon, two specific inhibitors of this category
48 13-metalloproteinase family enzyme-inhibitor phosphoramidon, using the senescence-accelerated mouse p
49  In the model, the zinc peptidase inhibitor, phosphoramidon, was docked in the active site.
50                              Enalaprilat and phosphoramidon were used to evaluate the impact of pepti
51 e for optimal activity and by sensitivity to phosphoramidon, which shows selectivity for ECE-2 over E

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